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Luteolin (LUT) is a natural flavonoid with low oral bioavailability with restricted clinical applications due to its low solubility. LUT shows significant anti-tumor activity in many cancer cells, including hepatocellular carcinoma (HCC). The most recent trend in pharmaceutical innovations is the application of phospholipid vesicles to improve the solubility of such hydrophobic drugs. Ethosomes are one of the most powerful phospholipid vesicles used to achieve that that target. In this study, LUT-loaded ethosomal nanoparticles (LUT-ENPs) were prepared by the cold method. Full factorial design and response surface methodology were used to analyze and optimize the selected formulation variables. Drug entrapment efficiency, vesicle size, zeta potential, Fourier transform infra-red spectroscopy, scanning electron microscopy, and cumulative percent drug released was estimated. The selected LUT-ENPs were subjected to further investigations as estimation of hepatic gene expression levels of GPC3, liver biomarkers, and oxidative stress biomarkers. The prepared LUT-ENPs were semi-spherical in shape with high entrapment efficiency. The prepared LUT-ENPs have a small particle size with high zeta potential values. The in vitro liver biomarkers assay revealed a significant decrease in the hepatic tissue nitric oxide (NO), malondialdehyde (MDA) content, and the expression of the GPC3 gene. Results showed a high increase in the hepatic tissue levels of glutathione (GSH) and superoxide dismutase (SOD). Histopathological examination showed a small number of hepatic adenomas and a significant decrease of neoplastic hepatic lesions after treatment with LUT-ENPs. Our results firmly suggest the distinctive anti-proliferative activity of LUT-ENPs as an oral drug delivery system for the treatment of HCC.

Introduction5-fluorouracil (5-FU) is the most widely used chemotherapeutic drug in treating colorectal cancer. However, its toxicity to normal tissues and tumour resistance are the main hurdles to efficient cancer treatment. MiR27-a promotes the proliferation of colon cancer cells by stimulating the Wnt/β-catenin pathway. The present study was conducted to examine whether quercetin (Q) combined with 5-FU improves the anti-proliferative effect of 5-FU on HCT-116 and Caco-2 cell lines through detection of the miR-27a/Wnt/β-catenin signalling pathway.Material and methodsCell viability in HCT-116 and Caco-2 cell lines following quercetin and 5-FU treatment alone and in combination for 48 hours was determined using the MTT assay. The flow cytometry, quantitative real-time polymerase chain reaction, and ELISA techniques were used.ResultsOur results showed that combination of quercetin and 5-FU exhibited greater cytotoxic efficacy than did 5-FU alone. Co-administration of both drugs either in combination 1 (1 : 1 Q: 5-FU) or in combination 2 (1 : 0.5 Q: 5-FU) enhanced apoptosis in HCT-116 and Caco-2 cells compared with 5-FU alone and significantly inhibited the expression of miR-27a, leading to upregulation of secreted frizzled-related protein 1 and suppression of Wnt/β-catenin signalling, which was confirmed by a significant decrease in cyclin D1 expression.ConclusionsQuercetin strongly enhanced 5-FU sensitivity via suppression of the miR-27a/Wnt/β-catenin signalling pathway in CRC, which advocates further research of this combination with the lower dose of 5-FU.

Introduction:The discovery of anticancer drugs from natural plants represents a large interest around the world. Ferulic acid (FA) is a natural phenolic acid has antitumor activity. Doxorubicin (DOX) is a potent chemotherapeutic agent used in the treatment of breast cancer, but its clinical uses are limited due to its toxic effects. This study aimed to evaluate the antitumour effect of FA and its nanosuspension (FA-NS) alone and in combination with DOX in Ehrlich solid tumour (EST)-bearing mice.Material and methods:Thirty-five female mice were divided into 7 groups: control, EST, FA, FA-NS, DOX, FA + DOX, and FA-NS + DOX. Proliferation, autophagy, apoptosis, angiogenesis, oxidative stress, and total antioxidant capacity (TAC) were investigated.Results:Our results showed that FA alone or in combination with DOX decreased tumour weight, proliferation, and angiogenesis by downregulating AKT and vascular endothelial growth factor receptor 2 levels, with marked elevation in autophagy and apoptosis indicated by upregulating Beclin-1, LC3-II, and caspase-3 levels. In addition, reduction of oxidative stress was indicated by decreased malondialdehyde and elevated TAC levels. Interestingly, the combination treatment mitigates DOX-induced different toxicities through the reduction of high levels of troponin-1, creatine kinase-MB, alanine transaminase, aspartate transaminase, urea, and creatinine.Conclusions:The combination of FA with DOX has the ability not only to promote the antitumour activity of DOX but also to ameliorate the side effects of DOX with more significant results when the FA was formulated by the nanotechnology.

Several studies have revealed that the combination of indomethacin, a nonsteroidal anti-inflammatory drug (NSAID), and vitamin D reduces the risk of common types of cancers. Nonetheless, research on the deal concentrations used to test the impact of vitamin D on colon cancer is deficient. Along these lines, the aim of the present study was to evaluate the possible role of indomethacin and vitamin D as a preventative as well as a therapeutic operator for colon cancer growth induced by dimethylhydrazine (DMH) in male Albino rats. Fifty male albino rats were utilized in this examination; five groups were assigned from the animals (10 animals each): i) control group considered healthy animals; ii) carcinogen group that received DMH only; iii) prophylactic group; iv) vitamin D and indomethacin-treated group; and v) 5-flurouracil (5-FU) group. Western blot technique was used to determine the expression of carcinoembryonic antigen (CEA) and platelet-derived growth factor (PDGF). Overexpression of CEA and PDGF was noted in the carcinogenic group, while expression of CEA and PDGF in the prophylactic, vitamin D and indomethacin and 5-FU groups were markedly reduced. There was a likewise decline in tissue caspase-3 activity and antioxidant parameters in the carcinogenic group, while, there was an increase in these markers in the 5-FU group as well as the prophylactic and vitamin D and indomethacin groups. The combination of vitamin D and indomethacin markedly reduced the incidence and severity of colon cancer. The molecular, biochemical and histopathological analysis related with the oral administration of vitamin D and indomethacin display its capacity to limit the frequency of colorectal cancer.

There is a growing interest in discovering natural sources of anti-cancer drugs. Sesamol (SES) is a phenolic compound with antitumor effects. The present study aimed to investigate the anticancer properties of SES and its nano-suspensions (SES-NS) combined with Epirubicin (EPI) in breast cancer (BC) using mice bearing a solid Ehrlich tumor. The study involved 35 female albino mice and investigated the effects of SES and EPI on tumor growth, proliferation, apoptosis, autophagy, angiogenesis, and oxidative stress. Methods including ELISA, qRT-PCR, and immunohistochemistry were utilized. The findings revealed reductions in tumor growth and proliferation using SES either alone or combined and evidenced by decreased AKT (AKT Serine/Threonine kinase1) levels, angiogenesis indicated by lower levels of VEGFR (vascular endothelial growth factor), and apoptosis demonstrated by elevated caspase3 and BAX levels. Furthermore, autophagy increased and was indicated by increased levels of beclin1 and lc3, along with decreased oxidative stress as evidenced by elevated TAC (total antioxidant capacity) and reduced MDA (malondialdehyde) levels. Interestingly, SES-NS demonstrated more significant effects at lower doses. In summary, this study underscores the potential of SES as a promising agent for BC treatment. Moreover, SES-NS potentiated the beneficial effects of EPI while mitigating its adverse effects.

Introduction The third most frequently diagnosed cancer and one of the highest causes of tumour deaths worldwide is colorectal cancer (CRC). The main objective of this study was to determine the role of microRNA-224 (miR-224) as well as microRNA-200a (miR-200a) in CRC. Phytic acid (PA) is a natural antitumour product that was reported to inhibit CRC and play a vital role as a chemopreventive agent against CRC. Material and methods We induced CRC in albino rats using 1,2-dimethylhydrazine (1,2-DMH). The miR-224, miR-200a, and -catenin expressions were determined. ELISAs were performed to investigate Bcl-2 expression, caspase-3 activity, and total tissue antioxidants. Finally, histopathological investigations were performed. Results We observed a chemoprotective role of PA. PA has a synergistic effect as an antitumour agent with oxaliplatin in CRC treatment. The miR-224, miR-200a, and -catenin expression, when treated with PA alone or with oxaliplatin, was decreased markedly in comparison with the positive control group. The histopathological investigations of colorectal tissues confirmed our molecular and biochemical findings. Conclusions Phytic acid possessed efficient anti-carcinogenic properties alone or with oxaliplatin against 1,2-DMH-induced CRC in rats through pathways of apoptosis, cell proliferation, and antioxidants.

Plants from the genus Astragalus are gaining attention for their pharmacological importance. However, the information available regarding the HPLC–MS/MS chemical profile of A. fruticosus is inadequate. In this study, we performed HPLC–MS/MS analysis using electrospray ionization (ESI) and atmospheric pressure chemical ionization (APCI). We tentatively identified 11 compounds in the A. fruticosus methanolic extract, including five flavonoidal and six saponin glycosides. The extract showed moderate antioxidant activity with 21.05% reduction in DPPH UV absorption. The preliminary cytotoxic screening against seven human cancer cell lines using 100 μg/mL extract showed prominent cytotoxic potential against colorectal cancer HCT–116 with 3.368% cell viability. It also showed moderate cytotoxic potential against prostate (DU–145), ovarian (SKOV–3) and lung (A–549) cancer cell lines with cell viability of 14.25%, 16.02% and 27.24%, respectively. The IC50 of the total extract against HCT–116 and DU–145 cell lines were 7.81 μg/mL and 40.79 μg/mL, respectively. The observed cytotoxicity of the total methanolic extract from the leaves against colorectal cancer might facilitate future investigations on cytotoxic agent(s) for disease management.

Thyroid cancer is among the most prevalent cancers with different types and stages. New markers are required for the prognosis and diagnosis of the disease. The present study aimed to detect the role of new markers, including galectin-3 (Gal-3) and thyroglobulin (TG), in the prognosis and staging of thyroid cancer. The study also investigated the potential apoptotic and inflammatory mechanisms involved in thyroid cancer through the determination of B-cell lymphoma 2 (Bcl-2), interleukin-8 (IL-8) and tumor necrosis factor α (TNFα) during the different stages of the cancer using a series of molecular methods. Histopathological and immunohistochemical examinations were also performed. A total of 300 subjects were classified into: 100 normal healthy subjects matched in age and sex, 100 patients with thyroid carcinoma stage I (T1N0M0) and 100 patients with thyroid carcinoma stage 2 (T2N1M1). Interestingly, the present study revealed a significant increase in the levels of TG and Gal-3 in thyroid cancer patients compared to the control group. Furthermore, the levels of Bcl-2, IL-8 and TNF-α significantly increased in the patient serum. The histopathological examination and immunohistochemical observations confirmed the molecular and hematological findings. Collectively, the present study concluded that serum TG and Gal-3 could be useful markers in the prognosis and staging of patients with thyroid cancer. Furthermore, the determination of Bax, Bcl-2, IL-8 and TNF-α levels constitute a major important marker for investigation of the mechanisms of apoptosis and inflammation in thyroid cancer. To our knowledge, this is the first study that used both galectin-3 and TG as tumor markers in the prognosis and differentiation between the different stages of cancer.

Introduction Soluble Toll-like receptor 4 (sTLR4) is a negative regulator of TLR4 signalling that has been reported in different diseases. In this study, we aimed to assess the serum levels of sTLR4 in hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC) and to investigate the correlation of sTLR4 with clinicopathological and biochemical parameters among HCV-related HCC patients and hepatitis C without HCC patients. Material and methods Fifty patients with HCV-related HCC, 50 patients with hepatitis C without HCC and 50 healthy control volunteers were enrolled. Clinicopathological and biochemical parameters were examined in all patients. Serum levels of sTLR4 were measured using enzyme-linked immunosorbent assay. Results A significant increase in serum sTLR4 was detected in patients with HCV-related HCC (4436.1 ±7089.8) (pg/ml) ± compared to the level in patients with hepatitis C without HCC (1561.4 ±532.0) (pg/ml) (p = 0.002) and the level in the control group (1170.38 ±159.42) (pg/ml) (p < 0.001). Serum sTLR4 was positively correlated with serum AST activity, serum direct bilirubin levels, serum alpha fetoprotein levels, tumour stages of HCC according to the Barcelona Clinic Liver Cancer staging system (BCLC), and the severity of liver cirrhosis according to the Child-Pugh classification among the patients with HCV-related HCC. The combination of serum alpha fetoprotein and serum sTLR4 increased the sensitivity of HCC detection to 76% and the specificity to 94%. Conclusions Serum sTLR4 may be a marker for HCC susceptibility among HCV-infected patients.